Homologies between T cell receptor junctional sequences unique to multiple sclerosis and T cells mediating experimental allergic encephalomyelitis.

M Allegretta; R J Albertini; M D Howell; L R Smith; R Martin; H F McFarland; S Sriram; S Brostoff; L Steinman

doi:10.1172/JCI117295

Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Department of Neurology and Neurological Sciences, Beckman Center, Stanford University School of Medicine, California 94305-5429.

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Published in Volume 94, Issue 1 on July 1, 1994
J Clin Invest. 1994;94(1):105–109. https://doi.org/10.1172/JCI117295.
© 1994 The American Society for Clinical Investigation

Published July 1, 1994 - Version history

The selection of T cell clones with mutations in the hypoxanthine guanine phosphoribosyltransferase (hprt) gene has been used to isolate T cells reactive to myelin basic protein (MBP) in patients with multiple sclerosis (MS). These T cell clones are activated in vivo, and are not found in healthy individuals. The third complementarity determining regions (CDR3) of the T cell receptor (TCR) alpha and beta chains are the putative contact sites for peptide fragments of MBP bound in the groove of the HLA molecule. The TCR V gene usage and CDR3s of these MBP-reactive hprt-T cell clones are homologous to TCRs from other T cells relevant to MS, including T cells causing experimental allergic encephalomyelitis (EAE) and T cells found in brain lesions and in the cerebrospinal fluid (CSF) of MS patients. In vivo activated MBP-reactive T cells in MS patients may be critical in the pathogenesis of MS.

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